A surprising new study reveals how the influenza virus rewires human gene expression to aid its own replication—offering a potential new path for antiviral therapy.
Key Points at a Glance
- The flu virus alters host cell gene regulation to promote its replication
- This manipulation weakens immune responses and enhances viral spread
- Researchers identified a drug that could counteract this viral tactic
- The findings could pave the way for novel antiviral strategies
For decades, influenza has remained a formidable opponent, shape-shifting through genetic mutations and evading immune defenses with seasonal precision. Now, scientists at the University of Gothenburg have uncovered a more insidious tactic in the virus’s arsenal: the ability to hack into our very DNA regulation systems. This unexpected discovery reveals that the influenza virus doesn’t just enter our cells to reproduce—it rewires how our genes function to tilt the biological battlefield in its favor.
At the heart of the finding is a complex molecule known as RNA polymerase II, an enzyme responsible for transcribing DNA into RNA—the fundamental process that drives protein production in human cells. When the influenza virus infects a cell, it manipulates this transcription process, subtly altering the way genes are expressed. Instead of a healthy, coordinated immune response, the host’s defenses are scrambled. Some genes that should be activated are silenced; others are turned on at inappropriate times. This molecular misdirection gives the virus an evolutionary edge, allowing it to replicate more efficiently while sidestepping the body’s initial immune alarms.
“We found that the influenza virus actively changes how host genes are expressed, and this has a direct effect on how well the virus can spread,” explains Professor Kristoffer Strålfors, one of the lead researchers behind the study. The implications of this are far-reaching. Traditionally, most antiviral treatments aim to attack the virus directly, but the virus’s ability to rapidly mutate often renders these drugs ineffective over time. This new insight into how the virus manipulates human gene expression suggests a completely different therapeutic strategy—strengthening the host rather than targeting the invader.
To explore this, the team tested the effect of a drug already approved for other uses, which is known to counteract the virus’s ability to interfere with host gene expression. In laboratory settings, the drug helped restore normal gene function, effectively blunting the virus’s impact on the immune system. Though the drug’s effect on human flu infections still needs to be verified through clinical trials, it marks a promising proof of concept. If successful, it could usher in a new generation of antiviral drugs that don’t try to outsmart the virus directly but instead deny it the tools it needs to corrupt our own biology.
This discovery also casts a spotlight on the growing field of “host-directed therapies”—an approach that has gained traction in recent years as scientists confront pathogens that evolve faster than traditional medicine can keep up. By understanding and defending the cellular processes that viruses exploit, researchers hope to create more resilient and longer-lasting treatments.
Moreover, the implications extend beyond influenza. Many viruses, including coronaviruses and HIV, rely on similar tactics to manipulate gene expression and suppress immune responses. The new findings could therefore help inform the development of broader-spectrum antiviral therapies.
In an era where viral pandemics are no longer once-in-a-generation anomalies but increasingly frequent threats, understanding the subtleties of viral manipulation is essential. The University of Gothenburg’s study is a reminder that viruses are not just external invaders—they are master manipulators that, once inside, use the very code of life against us. But armed with that knowledge, science is beginning to fight back—not just with stronger weapons, but with smarter ones.
Source: University of Gothenburg
